Research Group

  • Dr Dany Anglicheau, Principal Investigator
  • Prof. Phillipe Beaune, Co-Investigator
  • Prof. Xavier Jouven, Co-Investigator
  • Prof. Christophe Legendre, Clinical Collaborator


  • Necker Hospital, Paris, France


  • Non-invasive Biomarkers of Renal Allograft Fibrosis

Renal transplantation is the treatment of choice in end-stage renal failure. Short-term patient and graft outcomes have improved significantly over the years. However, these early benefits have had little impact on long-term graft survival. In the long-term, a progressive sclerotic process of the graft, formerly called chronic allograft nephropathy (CAN), remains the chief cause of kidney transplant failure. CAN is characterized by progressive sclerosis of the renal interstitium, glomeruli and vessels, and early CAN is present at a median of 3 months after transplantation, and by 1 year in 94.2% of patients. The current gold-standard test for the diagnosis of CAN remains a histological examination of the allograft biopsy. The biopsy procedures are invasive, complications may occur, and sampling errors may bias the histological diagnosis. The costs of these procedures also need to be considered. Early diagnosis of CAN, before the onset of graft dysfunction, would require multiple biopsies. A non-invasive test that could be diagnostic and/or prognostic is therefore urgently needed to detect early CAN in order to allow early and targeted therapeutic intervention and ultimately to improve the clinical management of transplant patients. Urinary-cell mRNA profiling has been successfully used to develop diagnostic biomarkers of acute rejection of renal allografts, however very few studies have evaluated this non-invasive approach for the diagnosis of allograft fibrosis. The purpose of this study is to explore the ability of the non-invasive approach of urinary-cell mRNA profiling to predict intragraft fibrogenic processes during the first year post-transplantation. We anticipate that we will develop a non-invasive approach for predicting fibrosis as a substitute for the invasive allograft biopsy procedure and that this will enable identification of patients at risk of chronic allograft dysfunction. The identification of a molecular signature of allograft fibrogenesis may allow specific therapeutic intervention to block this process.

Final Report